L18 Control of Circulation

Question 0

Resting Sympathetic tone

Answer 0

The amount of vascular smooth m contraction due to sympathetic nerve activity

Question 1

Basal arterial tone

Answer 1

The theoretical amount of basal vascular muscle contraction without neural/hormonal influences AT REST

Question 2

Passive/Active regulation

Answer 2

Passive mechanism is anything that goes TOWARDS the basal tone

Active mechanism is anything that goes AWAY FROM the basal tone

Active vasoconstriction = sympathetic
Active vasodilation = parasymp

Question 3

Alpha-1 adrenergic receptor

Answer 3

Causes VASOCONSTRICTION

NOT IN HEART OR BRAIN

Question 4

Beta-2 adrenergic receptors - 2 kinds

Answer 4

In heart, it is the secondary adrenergic receptor that stimulates HR and contractility

On vascular smooth m. and bronchioles, it VASODILATES
this is the receptor that viagra works on. It doesn’t affect the upper one

Question 5

Arterial baroreceptors

Answer 5

located in the walls of the aortic arch and the carotid sinus.

Less smooth m. than normal

Nerve terminals respond to stretch induced by ∆s in BP

Question 6

Baroreceptor reflex

Answer 6

When arterial P increases, the baroreceptors sense a lack in stretch, and this decreases vagal stimulation –> increase symp and decrease parasymp

vasoconstriction
increase HR
increase contractility

Baroreceptors have a threshold (this gets pushed up with hypertension) and they respond more to phasic, pulsatile ∆s in P
Static P change does not result in much response

Question 7

Chemoreceptors

Answer 7

These receptors are in the aortic and carotid bodies. They respond to low PO2, high PCO2, and acidosis.
This mainly works on the respiratory system but also has minimal effects on the heart; ultimately resulting in increases HR and constriction.

The brain and CV system respond to the chemoreceptors and turn on both PS and S nervous systems. However, the Chemoreceptors regulate the respiratory center, whose stretch receptors inhibit PS activity. Therefore HR increases

Question 8

Renin-Angiotensin-aldosterone regulation

Answer 8

When Arterial Pressure is low, this stimulates the afferent renal arterioles. Renin is released, which acts as a converter of Angiotensinogen –> Angiotensin I. ACE, from the lungs and kidney, converts Angiotensin I –> Angiotensin II. This is the final product that causes:
Aldosterone release –> absorb more Na and this more H2O
Vasoconstriction of renal and systemic vessels
Hypothalamus secretes ADH, which increases the permeability of the kidney so more H2O is reabsorbed.

All of this increases blood volume and pressure